Improvement In Mental Status Research Articles

7165 A Case of Severe Myxedema Coma with Levothyroxine Allergy

Abstract Disclosure: A. Rothstein Costris: None. A. Yaseen: None. S. Levy: None. Introduction: Myxedema coma is a life threatening condition with a mortality rate of 25-60%. Untreated, it can lead to fatal physiological changes. The treatment is thyroid hormone replacement therapy, alongside supportive care for complications. Clinical Case: A 65-year-old woman, who has been dealing with untreated hypothyroidism since 2012 and reported allergies to various levothyroxine brands, presented with falls, weakness, and exacerbated leg numbness. During the examination, she exhibited periorbital edema, non-pitting edema in the lower extremities, bradycardia, and hypothermia. The blood work revealed an elevation in TSH levels at 301 uIU/L (0.45-5.33 uIU/mL). The patient was administered IV Synthroid (200 mcg), Atropine, and Hydrocortisone due to concerns about myxedema coma. After four hours, the patient experienced angioedema and hypotension, necessitating intubation. This situation was complicated by a pulseless electrical activity (PEA) arrest. Following cardiopulmonary resuscitation and the administration of epinephrine, the patient achieved return of spontaneous circulation. The allergy team assessed the patient for potential anaphylactic shock from IV Synthroid. Subsequently, the patient was initiated onIV Liothyronine and Hydrocortisone, leading to improvement in mental status over a period of a few weeks, and no adverse effects were reported. Thyroid labs improved to TSH of 53 (0.45-5.33 uIU/mL), FT3 of 3.3 (2.5-4.4 pg/mL) and total T3 of 133 (87-178 ng/dl). Upon discharge, the patient was prescribed Liothyronine, with plans to perform a Levothyroxine desensitization test in the outpatient setting. Conclusion: Myxedema coma is an endocrine emergency. Patients usually present with deteriorating mental status, hypothermia, and multiple organ system abnormalities. The diagnosis relies more on the clinical presentation and physical examination than on laboratory results. Thyroid replacement therapy serves as the cornerstone of treatment, with a preference for T4 due to its greater availability and lower likelihood of adverse events compared to Liothyronine, which may increase the risk of mortality at higher doses. Despite associated risks, incorporating low doses of Liothyronine is still considered in treatment plans, driven by concerns about reduced T4 to T3 conversion in myxedema patients. Hypersensitivity reactions to Levothyroxine are uncommon but may manifest as widespread hives, swelling, eczema-like skin rashes, elevated body temperature, and compromised liver function, with only one case reporting an anaphylactic reaction to Levothyroxine. In summary, the potential for experiencing an anaphylactic reaction to Levothyroxine exists, highlighting the need to contemplate alternative treatments, such as Liothyronine. Desensitization methods can be considered once the patient's condition is stable. Presentation: 6/2/2024

Modafinil Therapy and Mental Status Following Aneurysmal Subarachnoid Hemorrhage: Comprehensive Stroke Center Analysis

Disorders of consciousness impair early recovery after aneurysmal subarachnoid hemorrhage (aSAH). Modafinil, a wakefulness-promoting agent, is efficacious for treating fatigue in stroke survivors, but data pertaining to its use in the acute setting are scarce. This study sought to assess the effects of modafinil use on mental status after aSAH. Modafinil timing and dosage, neurological examination, intubation status, and physical and occupational therapy participation were documented. Repeated-measures paired tests were used for a before-after analysis of modafinil recipients. Propensity score matching (1:1 nearest neighbor) for modafinil and no-modafinil cohorts was used to compare outcomes. Modafinil (100-200mg/day) was administered to 21% (88/422) of aSAH patients for a median (IQR) duration of 10.5 (4-16) days and initiated 14 (7-17) days after aSAH. Improvement in mentation (alertness, orientation, or Glasgow Coma Scale score) was documented in 87.5% (77/88) of modafinil recipients within 72hours and 86.4% (76/88) at discharge. Of 37 intubated patients, 10 (27%) were extubated within 72hours after modafinil initiation. Physical and occupational therapy teams noted increased alertness or participation in 47 of 56 modafinil patients (83.9%). After propensity score matching for baseline covariates, the modafinil cohort had a greater mean (SD) change in Glasgow Coma Scale score than the no-modafinil cohort at discharge (2.2 [4.0] vs.-0.2 [6.32], P= 0.003). A temporal relationship with improvement in mental status was noted for most patients administered modafinil after aSAH. These findings, a favorable adverse-effect profile, and implications for goals-of-care decisions favor a low threshold for modafinil initiation in aSAH patients in the acute-care setting.

Amantadine as an Aid to Extubation in Severe Acute Brain Injury: A Case Series.

For a subset of patients with severe acute brain injury (SABI) undergoing invasive mechanical ventilation, the primary barrier to successful extubation is depressed mental status. Amantadine is a neurostimulant that has been demonstrated to increase arousal and improve functional outcomes in patients with SABI. In this case series, we describe 5 patients with SABI and invasive mechanical ventilation who received amantadine as an agent to improve mental status to allow extubation. The primary barrier to extubation for all patients was depressed mental status. Median age was 77 (range 32 to 82). Primary diagnoses were ischemic stroke (n = 1), subdural hemorrhage (n = 2), intracerebral hemorrhage (n = 1), and traumatic brain injury (n = 1). Median Glasgow Coma Score was 7T prior to administration of amantadine and 10T on the day after amantadine was initiated, with improvements in eye-opening and motor response. Four patients displayed improvement in arousal and attention and were successfully extubated 1 to 4days after initiation of amantadine (median 2days). The fifth patient only displayed marginal improvement in mental status after starting amantadine, but was ultimately able to be extubated 7days later. Amantadine may improve the likelihood of or reduce the time to successful extubation in patients with SABI.

Successful Use of Therapeutic Plasma Exchange Following Red Blood Cell Exchange for Severe Acute Chest Syndrome: A Single Institution Experience

Introduction: Severe acute chest syndrome (ACS) is a potentially fatal complication of sickle cell disease (SCD) that can progress to multiorgan failure. Treatment includes red blood cell (RBC) exchange to improve oxygenation and reduce vaso-occlusion by decreasing the proportion of hemoglobin (Hb) S. Patients with poor response to RBC exchange are at high risk for mortality. Therapeutic plasma exchange (TPE) may be beneficial in cases of severe organ dysfunction refractory to RBC exchange. TPE is postulated to remove pro-inflammatory cytokines, reduce circulating free hemoglobin, and decrease complement products that contributes to vaso-occlusion and inflammation. The use of TPE for severe ACS and multiorgan failure has been rarely described in adult patients and is even less commonly described for pediatric patients. Aim: To describe use of TPE for the management of severe ACS with multiorgan failure in two pediatric patients and one young-adult patient who did not respond to standard medical management with RBC exchange transfusion. Methods: Case reports Case 1: A six-year-old male with homozygous SCD (HbSS) and moderate persistent asthma was admitted for ACS. His course was complicated by hypoxemia requiring intubation, oliguria, and hypotension. On hospital day 3, he underwent RBC exchange with four units of RBCs. Despite decrease of Hb S to 15%, he remained hypoxic on high ventilatory support and developed acute respiratory distress syndrome. After multidisciplinary discussion, TPE was trialed in hopes of improving oxygenation and reversing multiorgan dysfunction. He underwent 3 TPEs, each with 1.5 total plasma volume (TPV) using 5% albumin (days 4, 5 and 7). After a single session of TPE, his oxygenation saturations improved to the 90s, and his ventilator support was weaned. He was extubated on day 8 and was discharged on day 13 in stable condition. Case 2: A sixteen-year-old male with HbSS, recurrent hyper-hemolytic syndrome, and sickle cell hepatopathy was admitted for medical optimization before scheduled cholecystectomy. His Hb was raised pre-operatively with erythropoietin, in lieu of RBC transfusion, due to history of severe refractory hyper-hemolysis with transfusions. He underwent uncomplicated cholecystectomy on hospital day 2. On day 3, he developed ACS, septic shock, and an exacerbation of known hepatopathy. He was intubated and underwent RBC exchange with 8 units of RBCs. His Hb S decreased to 20% but he had no improvement in clinical status. High-dose steroids and TPE were then trialed. The use of TPE was dual purposed to reduce inflammatory cytokines contributing to systemic dysfunction and to prevent hyper-hemolysis following exchange transfusion. He underwent 3 TPEs each with 1.5 TPV using 5% albumin for three days (days 5, 6, and 7). Throughout his course of TPE, he was extubated (day 6), weaned off pressor support (day 6), and his liver dysfunction began to improve (day 7). He was discharged home on day 16. Case 3: A thirty-five-year-old female with HbSS without chronic complications was transferred from an outside hospital where she presented 3 days prior with ACS and progressive neurologic deterioration with minimal responsiveness. Imaging revealed diffuse pulmonary infiltrates and extensive cerebral micro emboli consistent with fat embolism syndrome. She underwent RBC exchange on the day of arrival to our facility (hospital day 4) with 5 units of RBCs. Her Hb S decreased to 20% but she had no improvement in neurologic function. After multidisciplinary evaluation, TPE was trialed alongside high-dose steroids. She underwent 5 TPEs each with 1.0 TPV using 5% albumin (days 5, 6, 8, 9, and 12). Shortly after initiating TPE, she began recovering neurologically with eye-opening, response to noxious stimuli, and tracking (day 6). After 3 days of TPE, CRP fell from 21 to 5 and ESR from 49 to 23 (day 8). She followed commands on day 10 and was taken off oxygen on day 15. She was discharged to a rehabilitation facility on day 30 with significant improvements in mental status, cognition, and functional abilities. Conclusions: TPE for three to five days should be considered in patients with severe ACS and multiorgan failure with high risk of mortality when standard management fails. The early initiation of TPE likely contributed to the successful recoveries of these three cases. Further studies are needed to delineate the role of TPE in the management of acute complications of SCD.

SAT196 COVID-19 Pneumonia And Primary Hyperparathyroidism Exacerbation

Abstract Disclosure: A. Khan: None. P. Rimal: None. M. Biggs: None. A. Ahmed: None. C. Musurakis: None. J.L. Gilden: None. A. Moid: None. Introduction: It is well known that COVID-19 virus damages the body by either inflicting the injury directly, or by initiating a systemic immune response, resulting in inflammation. Our case report explores how parathyroid glandular dysfunction and calcium levels (Ca) can be affected in a patient with active COVID-19 pneumonia. Clinical Case: A 58-year-old male, unvaccinated for COVID-19, with COPD, primary hyperparathyroidism (PHPT), chronic kidney disease, and ethanol use presented to the emergency room with confusion, vomiting, and lethargy. Preadmission medications included hydrochlorothiazide. Following a positive COVID-19 test, he was diagnosed with acute hypoxic respiratory failure secondary to COVID-19 pneumonia. After emergent treatment with BiPAP and IV steroids, he was transferred to the ICU, where he completed treatment with remdesivir, dexamethasone, and baricitinib. He was also treated for ethanol withdrawal. Notably, this patient had a history of chronic asymptomatic hypercalcemia secondary to PHPT with Ca prior to admission ranging from 10.9-13.6 mg/dl (nl=8.5-10.1mg/dl), PTH range 145-345 pg/ml (nl=14-65 pg/ml), creatinine (Cr) 1.2-1.4 mg/dl (nl= 0.67-1.17 mg/dl). On this admission, Ca was 12.2mg/dl, albumin 2.4 g/dl (3.4-5.0 g/dl), PTH 531 pg/ml, Cr 3.4 mg/dl, 25OH vitamin D 29.3 ng/mL (nl= 30-100 ng/mL). After fluids, Ca initially improved to 10.9mg/dl and Cr soon after normalized. Mental status also improved after hydration. However, Ca then rose significantly to 14.1mg/dl with mental status decline. IV zoledronic acid was administered, resulting in lowering serum calcium and improvement of mental status. Conclusion: This patient’s clinical course was notable for the improvement of Ca initially with hydration. However, a significant rise in Ca approaching parathyroid crisis range was seen shortly thereafter, despite normalization of Cr. Whereas hypocalcemia has been noted in most cases of Ca dysfunction associated with COVID-19 infection, in this case, we postulate that the COVID-19 infection may have triggered parathyroiditis, thus exacerbating the underlying PHPT. One such mechanism is the use of receptors like angiotensin-converting enzyme 2 (ACE2) and transmembrane protease serine 2 (TMPRSS2) by COVID-19 virus, which are found on endocrine glands including the parathyroid. Similarly, COVID-19 virus exerts its inflammatory effects using IL-6, which is also a key cytokine that causes hypercalcemia by stimulating bone resorption. Furthermore, COVID-19 infection is notorious for causing nausea/vomiting, and diarrhea, culminating in dehydration which worsens hypercalcemia. It is therefore necessary that physicians foresee impending complications of COVID-19 infection with concurrent parathyroid disease and take early steps to prevent and treat them. Presentation: Saturday, June 17, 2023

Nonconvulsive Status Epilepticus: A Review for Emergency Clinicians

BackgroundStatus epilepticus is associated with significant morbidity and mortality and is divided into convulsive status epilepticus and nonconvulsive status epilepticus (NCSE). ObjectiveThis review provides a focused evaluation of NCSE for emergency clinicians. DiscussionNCSE is a form of status epilepticus presenting with prolonged seizure activity. This disease is underdiagnosed, as it presents with nonspecific signs and symptoms, most commonly change in mental status without overt convulsive motor activity. Causes include epilepsy, cerebral pathology or injury, any systemic insult such as infection, and drugs or toxins. Mortality is primarily related to the underlying condition. Patients most commonly present with altered mental status, but other signs and symptoms include abnormal ocular movements and automatisms such as lip smacking or subtle motor twitches in the face or extremities. The diagnosis is divided into electrographic and electroclinical, and although electroencephalogram (EEG) is recommended for definitive diagnosis, emergency clinicians should consider this disease in patients with prolonged postictal state after a seizure with no improvement in mental status, altered mental status with acute cerebral pathology (e.g., stroke, hypoxic brain injury), and unexplained altered mental status. Assessment includes laboratory evaluation and neuroimaging with EEG. Management includes treating life-threatening conditions, including compromise of the airway, hypoglycemia, hyponatremia, and hypo- or hyperthermia, followed by rapid cessation of the seizure activity with benzodiazepines and other antiseizure medications. ConclusionsAn understanding of the presentation and management of NCSE can assist emergency clinicians in the care of these patients.

Management of Peri-mesencephalic Hemorrhage leading to acute hydrocephalus in an infant following Mild Trauma (P12-5.030)

<h3>Objective:</h3> To characterize etiology, risk factors, and management of peri-mesencephalic hemorrhage and severity of clinical presentation in pediatric populations <h3>Background:</h3> Peri-mesencephalic hemorrhage (PMH) is a form of mild subarachnoid hemorrhage (SAH) where the bleed is localized near the midbrain or just anterior to the pons without intraparenchymal or ventricular extension. It is typically a non-aneurysmal SAH (NASAH) with no clear source of bleeding after extensive vessel imaging including angiogram. Many hypotheses have been proposed such as spontaneous rupture of a perforating artery or an entirely venous source. Traumatic causes are rarely described. Outcomes are typically much better than aneurysmal SAH and other forms of NASAH with very low risk of rebleed, hydrocephalus, and little to no long-term neurologic deficits. <h3>Design/Methods:</h3> case study <h3>Results:</h3> An 8-month-old developmentally appropriate girl with no prior history of trauma who presented with three episodes of vomiting and lethargy 3–4 hours after a fall from standing position due to loss of balance while she was holding on to a folding chair. She fell backwards onto a tile floor and chair fell on top of her. CTH was obtained which showed prepontine and pontocerebellar hemorrhage spreading to ambient cisterns, IVH of the lateral and 3rd ventricles with acute noncommunicating hydrocephalus and no fracture. CTA with contrast and later MRI brain, MRA, and angiogram did not show any aneurysm or AVM per neurosurgery. EVD was placed with improvement in mental status. Repeat MRI brain was stable with very slight interval increase ventricle, and patient discharged home after 3rd ventriculostomy with no deficits. <h3>Conclusions:</h3> Though rare, trauma is a potential cause of PMH in pediatric populations and can present with acute hydrocephalus due to obstruction of ventricular system successfully treated with EVD placement and 3rd ventriculostomy with positive outcome. Hemorrhage may potentially be due to rupture of small perforating arteries through a sheering force. <b>Disclosure:</b> Dr. Johnson has nothing to disclose. Dr. Ming has nothing to disclose. Dr. Heshmati has nothing to disclose.

Acute Cerebellar Stroke of Unclear Etiology Complicated by Lemierre’s Disease and Papillary Thyroid Carcinoma (P2-10.001)

<h3>Objective:</h3> NA <h3>Background:</h3> Lemierre’s Disease is a rare condition that is usually caused by bacterial oropharyngeal infection, most common organism being Fusobacterium necrophorum, that is complicated by thrombophlebitis of the internal jugular vein. Below, is a case in which our stroke patient was found to have Lemierre’s Disease after obtaining a Karius panel. <h3>Design/Methods:</h3> Chart review for case report presentation. <h3>Results:</h3> 53-year-old female with no known medical history presented with headache, nausea, vomiting, fever and chills for three days. Lumbar puncture obtained was suggestive of bacterial source with elevated WBCs, nucleated cells with neutrophilic predominance, though her meningitis/encephalitis PCR panel was negative. Broad spectrum antibiotics was started. MRI brain showed a large ischemic right cerebellar infarct with mass effect. CTA of the head and neck, CT venography and MR venography showed nonocclusive thrombi of right proximal internal jugular vein and sigmoid sinuses. Repeat scans showed increasing hydrocephalus requiring EVD placement with eventual removal after improvement of mental status and serial imaging. Karius panel was positive for Fusobacterium nucleatum and porphyromonas gingivalis, and patient’s antibiotics was narrowed to reflect results. CT maxillofacial and neck showed extensive cervical lymphadenopathy and multiple periapical lucencies in teeth. IR guided cervical lymph node biopsies confirmed papillary thyroid carcinoma. Dentistry removed patient’s affected teeth. <h3>Conclusions:</h3> Although our patient had a large ischemic infarct, the more concerning issue was her concurrent meningitis from a bacterial source that caused a hypercoagulable state. With the Karius panel’s result, we promptly localized the infection and adjusted the patient’s antimicrobial management accordingly. Her clinical presentation continued to improve with treatment, and she was discharged to acute rehabilitation. Given the Karius panel’s rapid turnaround, in comparison to other metagenomic sequencing of CSF, we conclude that it is imperative to consider utilizing Karius panel testing for meningitis evaluation, especially in the setting of unremarkable meningitis/encephalitis PCR panel. <b>Disclosure:</b> Dr. Ho has nothing to disclose. Dr. Long has nothing to disclose. Dr. Kronfeld has nothing to disclose.

Rare Case of DPPX Encephalitis (P4-5.007)

<h3>Objective:</h3> N/A <h3>Background:</h3> Dipeptidyl-peptidase–like protein 6 (DPPX) antibody–associated encephalitis is a rare syndrome that includes weight loss, painful gastrointestinal symptoms, cognitive dysfunction, and CNS hyperexcitability. We describe a case of anti-DPPX encephalitis in a patient with painful GI symptoms and cognitive decline who underwent an extensive evaluation prior to diagnosis and treatment. <h3>Design/Methods:</h3> A 53 year old male presenting with recurrent emergency room visits with multiple seemingly unrelated symptoms. Symptoms occurred following a cruise and included skin discoloration, myalgias, and dyspnea. Respiratory symptoms resolved with standard bronchospastic treatment. He later developed dysesthesias, abdominal discomfort, and sixty pound weight loss. An extensive gastrointestinal evaluation was unremarkable. Persisting symptoms included anxiety and cognitive decline including apathy, memory impairment, and a persistent child-like demeanor, as well as exaggerated startle response. He underwent an inpatient psychiatric stay. His anxiety and depression slightly improved with psychotropic medications, however he did not return to his baseline positive demeanor. Symptoms of dysautonomia included episodic flushing and diaphoresis. Staring spells and unintelligible speech did not correlate with any simultaneous EEG recording. CSF resulted normal cell count and minimal increased protein (65 mg/dL). A lack of specific diagnosis and progressive decline prompted serum autoimmune antibody testing. Surprisingly, a positive anti-DPPX titer of 1:61440 was detected. Referred to oncology, the patient was treated sequentially with plasmapheresis and steroids, rituximab, and mycophenylate mofetil with a slight improvement in mental status over a period of weeks. <h3>Results:</h3> N/A <h3>Conclusions:</h3> Dipeptidyl-peptidase–like protein 6 (DPPX) is expressed in the hippocampus, cerebellum, striatum, and myenteric plexus, resulting in the unique presentation of DPPX antibody–associated encephalitis. This syndrome should be considered in patients with a triad of gastrointestinal symptoms, cognitive decline, and evidence of CNS hyperexcitability. Practitioners caring for patients with unknown CNS syndromes should have a low threshold for ordering CSF and serum CNS encephalitis panels, prompting earlier diagnosis. <b>Disclosure:</b> Dr. Pawate has nothing to disclose. Dr. Sandhu has nothing to disclose. Dr. Weisman has received personal compensation in the range of $500-$4,999 for serving on a Speakers Bureau for Biogen. Dr. Small has received personal compensation in the range of $500-$4,999 for serving on a Speakers Bureau for Alexion.

Abstract Number ‐ 215: Distinct presentation of RCVS and PRES co‐existence and overlap of their pathophysiology

Introduction Reversible cerebral vasoconstriction syndrome (RCVS), is characterized by reversible segmental and multifocal vasoconstrictionof cerebral arteries leading to infarcts and cytotoxic edema. Posterior reversible encephalopathy syndrome (PRES) is characterized by vasogenic edema predominantly in the parieto‐occipital regions associated with acute onset encephalopathy, seizures, headache, and visual disturbances.Whether PRES and RCVS are independent syndromes and sometimes overlapped or part of a continuum process, these theories are still debated. We report a case of a patient with distinct overlapping of RCVS and PRES. Methods Case Report Results 52‐year‐old woman with past medical Hx of Hypertension, Diabetes, Migraines and cocaine use, initially presented with hypertensive emergency andsubacute headaches with worsening confusion. Initial CT head was negative for bleed but showed evolving subcortical hypodensities in the right parietal and left frontal lobes. CTA head and neck showed multifocal intracranial irregularities of bilateral ACAs and MCAs with paucity of left anterior M2 branch, left V3/V4 steno‐occlusion. This vasculopathy and clinical presentation is very consistent with RCVS.MRI of brain showed multiple acute / subacute punctate infarcts in the left corona radiata, bilateral basal ganglia, right greater than left thalami, right dorsal pons, right mesial temporal lobe, bilateral occipital regions. Vasogenic edema was noted in the bilateral border zone regions, right parietal being most prominent with some contrast enhancement. The MRI showed vasogenic edema and cytotoxic edema with multiple infarcts which is consistent with PRES and RCVS vasculopathy. CSF analysis was negative for pleocytosis and showed mildly elevated protein. The patient was started on Verapamil and Aspirin and Atorvastatin for secondary stroke prevention. With improvement in mental status was discharged to Rehab. Conclusions The pathophysiological mechanisms of PRES and RCVS are still unknown. Theories whether RCVS and PRES are independent syndromes and sometimes overlap or part of spectrum, are still debated. However, some common characteristics make conceivable a common origin linked with impaired cerebral autoregulation, endothelial dysfunction, and BBB breakdown. Increased clinical awareness of their co‐existence may help in quickerdiagnosis and treatment.

A curious case of confusion

A curious case of confusion

479: MULTIORGAN FAILURE AND EHRLICHIOSIS: TIMELY TREATMENT IS THE KEY TO SUCCESS

Introduction: Ehrlichia chaffeensis is the causative organism for human monocytic ehrlichiosis (HME). HME is the most common life-threatening tick-borne disease with an overall mortality of more than 2.5%. HME can present as multiorgan failure making the timely diagnosis challenging. We present a case of HME presenting with multiorgan involvement being treated with doxycycline. Description: A 75-year-old female with a past medical history of atrial fibrillation presented with complaints of dizziness and fatigue. She was a resident of Central Virginia and was out in the woods for yoga 2 weeks ago. On presentation, she had a heart rate of 61 BPM, Blood Pressure of 79/44, Respiratory rate of 22/min, and Saturation of 96% on room air. On the physical examination, she was drowsy and confused. There was no rash or erythema. Xray of the chest was without any focal consolidation. CT head did not show any acute intracranial pathology. Initial blood labs showed pancytopenia, transaminitis, and raised creatinine. She also had CPK of 2017 u/l, ferritin >40,000 ng/ml, and an LDH of 2141 u/l. She was volume resuscitated and started on broad-spectrum antibiotics. Blood cultures were sent. The patient did not have any improvement in mental status and the initial infectious workup was negative. A Lumbar puncture was performed that showed normal cell count. Based on her history and concern for tick-borne disease her antibiotics were changed to doxycycline and serologic studies were sent. Due to high ferritin and pancytopenia, she underwent a bone marrow biopsy to rule out secondary hemophagocytic lymphohistiocytosis which showed no hemophagocytic cells and normal bone marrow. Her ehrlichia chaffeensis PCR resulted positive. She was continued on doxycycline with gradual improvement in mental status, liver function, and blood cell count. Discussion: HME can present as liver failure, myositis, renal failure, pancytopenia, and nervous system involvement. HME can rarely also present with seizures, the role of LP is unclear as it can be normal in HME encephalitis as it was in our patient. PCR and serological studies are diagnostic. Patients with multiorgan involvement should be started on doxycycline if HME is suspected and supported by history. Patients are expected to make full recovery after appropriate treatment.

1161: CANNABIS INTOXICATION: A RARE CAUSE OF LACTIC ACIDOSIS

Introduction: Lactic acidosis is common in critically ill patients and has a variety of etiologies. While sepsis, hemorrhage, and shock are the most common causes of lactic acidosis, a subset of patients have no obvious cause. Drug and medication toxicity remains a rare cause of lactic acidosis that providers often fail to recognize. Here, we present a rare case of lactic acidosis due to acute marijuana intoxication. Description: A 26-year-old male with no prior history of marijuana use was brought into the emergency department with complaints of shortness of breath and palpitations after ingesting ice cream containing cannabis. Per EMS, the patient was found screaming for help due to his symptoms but evidently with altered mentation. On arrival, the patient was febrile to 101.9 F with a heart rate of 156 bpm; he was normotensive and saturating well on room air with a normal respiratory rate. Laboratory studies were significant for an elevated lactate level of 4, a white blood cell count of 11, and a urine drug screen positive for THC. The patient was given empiric broad-spectrum antibiotics, 2 liters of lactated ringer’s, and IV naloxone with no improvement in mental status. Studies and physical examination did not reveal any source of infection. After careful monitoring, the patient’s mental status recovered and lactic acid cleared with supportive measures. The patient was later discharged safely home with appropriate follow-up. Discussion: Poisoning is one of the leading causes of injury-related casualties in the United States, and lactic acidosis is a widely used predictor to stratify patients who are at increased risk for mortality. Elevated lactate levels result from an imbalance between lactate metabolism and production. Synthetic cannabinoids have been established as rare causes of lactic acidosis. Chronic marijuana use has been associated with lactic acidosis by way of thiamine deficiency and gastrointestinal beriberi corrected promptly with vitamin administration. There are no reported cases linking acute marijuana use and lactic acidosis development in the absence of infection, hemodynamic compromise, or seizures. It is important to keep drug ingestion and intoxication in mind as important causes of lactic acidosis in the absence of other apparent etiologies.

PSAT334 An Unusual Case of Thyroid Storm in a Patient with Schizophrenia-A Diagnostic Dilemma

Abstract Introduction Thyroid storm represents life threatening endocrine disorder that requires early recognition and treatment due to significant mortality rates. Case reports in which diagnosis of thyroid storm was delayed secondary to acute psychotic symptoms mainly consisting of auditory hallucinations, delusions, and violent behavior have been published. This case serves to illustrates that even in patients with schizophrenia acute psychiatric disorder can be early manifestation of life-threatening endocrine disorder. Clinical case We present a case of 25-year-old male with history of schizophrenia who was brought to hospital after he was found down, disoriented, with auditory hallucinations. Associated symptoms included diarrhea and abdominal pain. On physical exam patient was found to have altered mental status, proptosis, tachycardia, diaphoresis, and warm and moist skin. Due to suspicion for worsening schizophrenia patient was evaluated by psychiatry and was found to have active suicidal ideation. Thyroid function tests (TFTs) was significant of elevated fT4 and T3 (fT4 &amp;gt; 5.0 ng/dl, T3 6.5 ng/dl) and suppressed TSH (0.020 µIU/ml). Burch-Wartofsky Point Scale was suggestive of impending thyroid storm and endocrinology was consulted after which treatment with methimazole, dexamethasone, propranolol, and potassium iodide (Lugol's solution) was started. On second day of treatment patient had significant improvement in mental status with resolution of auditory hallucination, suicidal ideation, and tachycardia with complete return to his baseline mental status on the third day of hospital stay. At the end of hospital course TFTs also showed decrease in fT4 and T3 and patient was discharged on methimazole and propranolol as well as paliperidone for treatment of schizophrenia. When patient was seen during outpatient follow-up, he was free of any psychiatric symptoms. Conclusion Mental status changes due to thyroid storm versus acute worsening of schizophrenia is hard to differentiate. Our case shows that even in the patients with prior psychiatric history, thyroid storm should be highly on differential diagnosis especially when patients are presenting with acute worsening of symptoms. In this case high suspicion for thyroid storm and early treatment in first 24h of the presentation lead to favorable outcome of this life-threatening condition. As thyroid storm is clinical diagnosis, high suspicion, use of Burch-Wartofsky Point Scale and early measurement of TFTs can help physicians distinguish thyroid storm from primary neuropsychiatric presentation. Presentation: Saturday, June 11, 2022 1:00 p.m. - 3:00 p.m.

Vocational training of health mediators of primary care teams improves their sense of coherence

Abstract Background A Primary Care Model Programme had been implemented in Hungary between 2013-2017 in which group practices were established that employed - among others - nonprofessional health workers (health mediators, similar to community health workers) to facilitate access for the most disadvantaged population groups. The health of mediators, themselves mostly disadvantaged ethnic Roma, was monitored every odd year of the Programme. Methods A repeated cross-sectional health interview survey had been implemented inviting all health mediators who were employed at the time of the survey. The same questionnaire was used in all 3 surveys with items from the European Health Interview Survey 2009 and validated versions of other scales. Results Positive changes occurred in the health status of mediators during 5 years of follow-up. Significant improvement in mental health occurred among those who completed on-the-job vocational training. By 2017, significant increase in sense of coherence was observed among those who obtained vocational qualification as opposed to those who did not. The proportion of highly stressed mediators showed a significant increase among those with no vocational training. Improvement was detected in all mediators in health awareness, dysfunctional attitudes, psychological stress and smoking prevalence. Conclusions Significant improvement in mental status among those who obtained on-the-job vocational qualification were observed during follow-up of ethnic Roma health mediators in the programme in which they were equal members of the primary health care team. Employment of health mediators in primary care teams not only contributed to improving access to care for disadvantaged groups but also improved the mental health of mediators themselves. Key messages • Nonprofessional health mediators are important members of primary care teams servicing disadvantaged populations. • Significant improvement in mental status during 5 years of follow-up occurred among Roma health mediators who received vocational training and were equal members of primary health care teams.

S3111 An Unusual Case of Acute Liver Failure Secondary to Autoimmune Hepatitis (AIH) From Drug-Induced Liver Injury (DILI)

Introduction: A broad differential diagnosis and detailed workup is necessary in the evaluation of acute liver failure, as the below case demonstrates. Case Description/Methods: A 68-year-old Caucasian man presented to the ED complaining of chronic right lower quadrant pain, worsening over the last few weeks. He reported taking up to 20 tablets of naproxen a day. Review of systems was positive for diffuse pruritis of recent onset. Past medical history consisted of COPD, inguinal hernia status post mesh repair, knee osteoarthritis and a cholecystectomy. He endorsed daily tobacco use and minimal alcohol intake. Medications consisted of Albuterol inhaler and Naproxen. He had been diagnosed with a urinary tract infection one month prior that was treated with a ten-day course of Cephalexin. Exam was notable for diffuse excoriation and right upper/lower quadrant tenderness. Initial labs demonstrated creatinine 0.87, AST 2635, and ALT 887, with the remainder of his comprehensive metabolic panel being normal. Contrasted CT scan of the abdomen and pelvis revealed no abnormalities. A right upper quadrant ultrasound was notable for left sided intrahepatic biliary dilatation. Over the next day, his mentation worsened, with repeat labs notable for bicarbonate 13, creatinine 3.08, AST 12050, ALT 3950, total bilirubin 2.4 with direct bilirubin 1.5, INR 3.11 and ammonia 164. A broad infectious workup was unremarkable including negative viral hepatitis serologies. Smooth muscle antibody was weakly positive at a low titer of 1:20. Anti-nuclear and anti-mitochondrial antibodies were negative. Serum IgG level was normal. Endoscopic retrograde cholangiopancreatography revealed a severe left intrahepatic biliary stricture with resulting stent placement into the left hepatic duct. Bile duct brushing was negative for atypical cells. Liver biopsy demonstrated centrilobular necrosis and parenchymal collapse with focal bridging necrosis and mixed inflammatory infiltrate. A diagnosis of AIH secondary to DILI leading to acute liver failure was made, with either Naproxen or Cephalexin being the inciting drugs. Discussion: He was started on a prednisone taper and showed improvements in mental status and kidney and liver function on lab-work prior to discharge. Labs obtained on clinic follow-up one month after discharge revealed complete resolution of his kidney and liver injury. This case illustrates a rare clinical entity as neither Naproxen nor Cephalexin are classically associated with causing AIH or acute liver failure.

Changes in adipokine concentrations in antidepressant-resistant bipolar depression after ketamine infusion and electroconvulsive therapy

Objectives This study attempts to assess the concentration of two opposite-acting adipokines (anti-inflammatory adiponectin and pro-inflammatory resistin) in antidepressant-resistant patients undergoing ketamine infusion (KI) and electroconvulsive therapy (ECT). Methods The study group comprised 52 patients hospitalised due to episodes of depression in the course of bipolar disorders. The Hamilton depression scale was used to assess the intensity of the depression symptoms before starting therapy and one day after its completion. The serum concentration of adipokines was determined before and after the therapeutic intervention using an ELISA method. Results Baseline adipokine levels differed between patients receiving KI and ECT therapy. Regardless of the procedure used, these levels changed after treatment, with the nature of these changes being different. In the case of KI, the adiponectin levels increased, and resistin levels decreased. In contrast, after ECT, the concentrations of both adipokines decreased. Changes in adipokine concentrations correlated with improvement in mental status, as assessed by the Hamilton Rating Scale, type of bipolar disorder, and gender. Conclusions Adipokines remain interesting candidate biomarkers in assessing the state and course of the disease depending on the therapeutic procedure applied. However, the relatively small study group and limited original research available for discussion justify further investigation.

Hyperammonemia Post Lung Transplant: A Rare and Fatal Complication

Introduction Among the extra pulmonary complications associated with lung transplantation, severe hyperammonemia has been reported as a rare and fatal complication with an incidence of up to 4% and a fatality rate of 67% in some case series. We present a case report of a patient who underwent bilateral lung transplantation and developed severe hyperammonemia in his immediate post-operative course. Case Report A 66 year old male with past medical history of idiopathic pulmonary fibrosis was referred to our center for evaluation for bilateral lung transplantation. He underwent a technically uncomplicated successful procedure and his immediate post-operative course was complicated by metabolic acidosis and acute renal failure. On post op day 4 he developed mental status changes and was noted to have elevated plasma ammonia of 154 mcmol/L. Laboratory and imaging studies were negative for acute hepatic dysfunction. A head CT was negative for cerebral edema or acute findings. He was started on rifaximin, lactulose enemas and via nasogastric tube, in addition to empiric macrolide therapy. Despite these interventions his mental examination and ammonia level did not improve in the following 24 hours. He was initiated on L-arginine, sodium benzoate and levocarnitine for possible undiagnosed glutathione synthase deficiency. Continuous renal replacement therapy (CRRT) for more rapid ammonia clearance was also started. He required CRRT for 5 days with gradual improvement in mental status. CRRT was discontinued once plasma levels normalized. He was slowly weaned off the above pharmacological interventions in the ensuing 3 weeks. He was discharged to inpatient rehabilitation without the need of any medical therapies for hyperammoenmia on post op day 30. He remained well for a period of 4 years post-transplant and eventually succumbed to chronic lung allograft dysfunction. Summary The primary underlying mechanism for post transplant hyperammonemia remains unknown, but several risk factors have been linked to this condition. The most commonly reported are disseminated opportunistic infection with ureaplasma or mycoplasma, high nitrogen loads, pulmonary hypertension and hepatic glutamine synthetase deficiency. Treatment regimens are multimodal but overall aimed at reducing ammonia levels and providing neuroprotection. Early initiation of treatment is paramount for improving survival and outcomes. Among the extra pulmonary complications associated with lung transplantation, severe hyperammonemia has been reported as a rare and fatal complication with an incidence of up to 4% and a fatality rate of 67% in some case series. We present a case report of a patient who underwent bilateral lung transplantation and developed severe hyperammonemia in his immediate post-operative course. A 66 year old male with past medical history of idiopathic pulmonary fibrosis was referred to our center for evaluation for bilateral lung transplantation. He underwent a technically uncomplicated successful procedure and his immediate post-operative course was complicated by metabolic acidosis and acute renal failure. On post op day 4 he developed mental status changes and was noted to have elevated plasma ammonia of 154 mcmol/L. Laboratory and imaging studies were negative for acute hepatic dysfunction. A head CT was negative for cerebral edema or acute findings. He was started on rifaximin, lactulose enemas and via nasogastric tube, in addition to empiric macrolide therapy. Despite these interventions his mental examination and ammonia level did not improve in the following 24 hours. He was initiated on L-arginine, sodium benzoate and levocarnitine for possible undiagnosed glutathione synthase deficiency. Continuous renal replacement therapy (CRRT) for more rapid ammonia clearance was also started. He required CRRT for 5 days with gradual improvement in mental status. CRRT was discontinued once plasma levels normalized. He was slowly weaned off the above pharmacological interventions in the ensuing 3 weeks. He was discharged to inpatient rehabilitation without the need of any medical therapies for hyperammoenmia on post op day 30. He remained well for a period of 4 years post-transplant and eventually succumbed to chronic lung allograft dysfunction. The primary underlying mechanism for post transplant hyperammonemia remains unknown, but several risk factors have been linked to this condition. The most commonly reported are disseminated opportunistic infection with ureaplasma or mycoplasma, high nitrogen loads, pulmonary hypertension and hepatic glutamine synthetase deficiency. Treatment regimens are multimodal but overall aimed at reducing ammonia levels and providing neuroprotection. Early initiation of treatment is paramount for improving survival and outcomes.

Tetanus Presented as Acute Abdomen

Tetanus is commonly seen in the emergency department with a puncture wound. This is an unusual presentation of tetanus without an open wound. A 59 year old male with a past history of hypertension, hepatitis C, prior injection drug use, and homeless presented to the emergency department with altered mental status and hyperthermia with fever of 105 F on a hot July afternoon. Patient was found in his car sleeping. Initially, the patient declined medical care, but was later found unresponsive with a methadone bottle next to him. Given Narcan on field with improvement of mental status. Patient developed acute ridged abdominal pain. A CT scan raised concern for acute abdomen, with portal venous gas, and intestinal pneumatosis. Surgery consulted and was concerned for ischemic colon with perforation. Vancomycin, ceftriaxone and metronidazole were given. Emergency exploratory laparotomy was performed with a small serosal injury on colon repaired with suture. Blood culture came back positive for Clostridium tetani and Mobiluncus curtisii. Infectious disease consulted. Felt tetanus cannot be ruled out. Patient was given tetanus immune globulin (TIG), metronidazole and later tetanus vaccine. Patient has fully recovered, tolerates oral diets, and has been discharged to a nursing facility without any neurological deficit. Tetanus is a neurological disorder caused by the tetanus toxins produced by clostridium tetani, which is a gram positive obligate anaerobes commonly found in soil. It is relevant to note that this bacterium can also be found inside the gut of animals and humans. The disease is well characterized by ancient Greeks, and common symptoms include trismus (“lockjaw”), opisthotonos, and a board-like rigid abdomen. Incubation is usually 7-21 days and this disease is usually prevented by vaccination. This case is unusual because there is no open wound and PE is limited due to patient’s overdose on opiates (methadone). Possible cause for this particular case may be that since there was no open wound, the blood could have been seeded by the perforated bowel because they may also be found in the gut. The patient was given metronidazole as part of Tx for acute abdomen, which happens to also be a treatment for tetanus. Diseases can be presented atypically. This case illustrates the importance of differential diagnosis when considering treatments in any pathology.

Prehospital Intranasal Glucagon for Hypoglycemia

Background Prehospital hypoglycemia is usually treated with oral or intravenous (IV) dextrose in a variety of concentrations. In the absence of vascular access, intramuscular (IM) glucagon is commonly administered. Occupational needle-stick injury remains a significant risk while attempting to obtain vascular access or administer medications intramuscularly in the prehospital setting. We sought to determine if intranasal (IN) glucagon is effective in the prehospital treatment of hypoglycemia. Methods We performed a retrospective analysis of all consecutive cases where recombinant glucagon was administered IN by paramedics from January 1, 2015 through December 31, 2020. Excluded were cases without pre or post administration blood glucose documentation, and cases where another form of treatment for hypoglycemia was administered at any time during the EMS encounter. The primary outcome was clinical response to IN glucagon documented by paramedics; secondary outcomes included pre and post administration blood glucose values. Results Out of 44 cases that met study inclusion criteria, 14 patients (32%) had substantial improvement, 13 patients (30%) had slight improvement, and 17 patients (38%) had no improvement in mental status after administration of IN glucagon. In cases with substantial improvement (n = 14), the mean pre administration blood glucose was 33.8 mg/dl and the mean post administration blood glucose was 87.1 mg/dl (mean increase 53.3 mg/dl, 95% CI: 21.5 to 85.1). In cases with slight improvement (n = 13), the mean pre administration blood glucose was 23.9 mg/dl and the mean post administration blood glucose was 53.8 mg/dl (mean increase 29.9 mg/dl, 95% CI = 2.9 to 56.9). In case with no improvement (n = 17) the mean pre administration blood glucose was 30.1 mg/dl and the mean post administration glucose was 33.1 mg/dl (mean difference 3.1 mg/dl, 95% CI: −10.1 to 3.9). Conclusion Intranasal administration of recombinant glucagon for hypoglycemia resulted in a clinically significant improvement in mental status and a corresponding increase in blood glucose levels in select cases in the prehospital setting.